DOCSLIB.ORG

1999 Handbook

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
1999 Handbook The Australian Short Course on Intensive Care Medicine 1999 Handbook The Australian Short Course on Intensive Care Medicine 1999 Handbook Editor L.I.G. Worthley Published in 1999 by The Australasian Academy of Critical Care Medicine Department of Critical Care Medicine Flinders Medical Centre, Bedford Park South Australia 5042 ISSN 1327-4759 1999 The Australasian Academy of Critical Care Medicine Requests to reproduce original material should be addressed to the publisher. Printed by Gillingham Printers Pty Ltd 153 Holbrooks Road Underdale South Australia 5032 CONTENTS Page Chapter 1. Cardiac anatomy 1 Chapter 2. Physiology of myocardial contractility 7 Chapter 3. Cardiac output and oxygen delivery 25 Chapter 4. The autonomic nervous system 49 Trainee Presentations 67 Index 131 iii iv 1999 SHORT COURSE PROGRAMME March 22nd 23rd 24th 25th 26th FMC QEH RAH RAH FMC 0815 Travel to Travel to Travel to FMC QEH FMC 0900 Lecture Interactive Lecture Lecture Lecture Examination of Management of Diagnosis & ] the critically ill Clinical adult neurotrauma of nosocomial Acute liver patient vignettes J.M pneumonia failure L W. L.W. M.C. A.H 1015 Lecture Interactive Clinical cases Interactive Interactive Biochemistry, J.M M.C In defence of Blood gases, ---------------------- Clinical cases Acid base & Blood Pressure Bacteriology Trauma vignettes Blood gases A.B B.V. B.G. M.F L.W 1130 Clinical cases Interactive Lecture Interactive Interactive A.V A.H B.V L.W --------------------- X-rays Organ donation Pathology, X Presentat’ns Respiratory rays, ECG’s assistance in airflow L.W. R.Y M.F L. W obstruction A.B 1245 Lunch Travel to WCH 1400 Interactive Lecture Lecture Lecture Common ECG's Outcome ARDS update paediatric Prediction ICU problems L.W J.M M.C N.M 1515 Lecture Interactive Clinical cases Short questions Understanding M.F R.Y Fluid & Asthma and ---------------------- N.M. A.S Electrolytes COPD update Trauma vignettes L.W R.R B.G. 1630 Interactive Lecture Lecture Pharmacological Path Forms Biochemistry support of the in the ICU circulation L.W P.P J.M 1745 Travel To RAH Travel to ** RAH FMC = Flinders Medical Centre QEH = Queen Elizabeth Hospital WCH = Women’s and Children's Hospital RAH = Royal Adelaide Hospital **DINNER: Thursday 25th 7 pm: 22 William St, Hawthorn (registrants at RAH accommodation block will be picked up at 6.45 pm) v REGISTRANTS Code Name Institution * 1. Dr. P. Glover Intensive Care Unit, Flinders Medical Centre, SA * 2. Dr. D. Cooper Intensive Care Unit, John Hunter Hospital, NSW * 3. Dr. K. H. A. Leung Intensive Care Unit, Queen Elizabeth Hospital, Hong Kong * 4. Dr. N. Ramakrishnan Intensive Care Unit, St Vincent’s Hospital, Victoria * 5. Dr. M. Clifford Intensive Care Unit, Royal Children’s Hospital, Victoria * 6. Dr. C. McCalman Intensive Care Unit, Waikato Hospital, New Zealand * 7. Dr. M. Chinthamuneedi Intensive Care Unit, Women’s & Children’s Hospital, SA * 8. Dr. A. McKee Intensive Care Unit, Green Lane Hospital, New Zealand * 9. Dr. P. Kruger Intensive Care Unit, Princess Alexandra Hospital, Queensland * 10. Dr. P. Harrigan Intensive Care Unit, Royal Perth Hospital, WA * 11. Dr. V. Yeo Intensive Care Unit, Prince of Wales Hospital, Hong Kong * 12. Dr. R. Holland Intensive Care Unit, Napean Hospital, NSW * 13. Dr. N. Widdicombe Critical Care Unit, Flinders Medical Centre, SA * 14. Dr. M. Hayden Intensive Care Unit, Sir Charles Gairdner Hospital, WA * 15. Dr. B. McFadyen Intensive Care Unit, John Hunter Hospital, NSW * 16. Dr. J. Yeo Intensive Care Unit, Pamela Joude Nethersole Hospital, Hong Kong * 17. Dr. K. Quan Intensive Care Unit, Westmead Hospital, NSW * 18. Dr. P. Seal Intensive Care Unit, St. Vincent’s Hospital, Victoria * 19. Dr. J. Foy Department of Critical Care Medicine, Auckland, NZ * 20. Dr. D. Gattas Intensive Care Unit, Royal Prince Alfred Hospital, NSW * 21. Dr. T. Leong Intensive Care Unit, The Alfred Hospital, Victoria 22. Dr. C. Simpson Intensive Care Unit, Waikato Hospital, New Zealand 23. Dr. G. Howard Intensive Care Unit, Christchurch Hospital, New Zealand 24. Dr. T. W. Lim Intensive Care Unit, Royal Perth Hospital, WA 25. Dr. D. Connor Intensive Care Unit, Manning Base Hospital. NSW 26. Dr. R. Fitzgerald Intensive Care Unit, North Shore Hospital, New Zealand 27. Dr. P. Meuer Intensive Care Unit, North Shore Hospital, New Zealand 28. Dr. P. Jowitt Intensive Care Unit, Mildura Base Hospital, Victoria 29. Dr. A. Harvey Intensive Care Unit, Princess Alexandra Hospital, Queensland 30. Dr. M. Kluger Intensive Care Unit, North Shore Hospital, New Zealand 31. Dr. D. Sidebotham Intensive Care Unit, Green Lane Hospital, New Zealand 32. Dr. K. Tan Intensive Care Unit, Austin & Repatriation Medical Centre, Victoria 33. Dr. C. Lee Intensive Care Unit, Westmead Hospital, NSW 34. Dr. A. Love Intensive Care Unit, North Shore Hospital, New Zealand 35. Dr. B. King Intensive Care Unit, Nelson Hospital, New Zealand 35. Dr. G. Auzinger Intensive Care Unit, Alfred Hospital, Victoria FACULTY FMC QEH RAH WCH Dr. L. Worthley (L.W) Dr. M.O’Fathartaigh (M.O’F) Dr. J. Myburgh (J.M) Dr. N. Matthews (NM) Dr. A. Vedig (A.V) Dr. J. Moran (J.M) Dr. P. Thomas (P.T) Dr. A. Slater (A.S) Dr. A. Bersten (A.B) Dr. S. Peake (S.P) Dr. B. Griggs (B.G) Dr. A. Holt (A.H) Dr. R. Ruffin (R.R) Dr. R. Young (R.Y) Dr. E. Everest (E.E) Dr. M. Finnis (M.F) Dr. M. Chapman (M.C) GUEST Dr. B.Venkatesh (B.V) * registrants willing to undergo a 'clinical' vi PREFACE A working knowledge of the basic sciences of, anatomy, physiology and pharmacology is the basis for the understanding and management of the critically ill patient. This year the Australian Short Course on Intensive Care Medicine handbook has included a cursory look at the basic sciences of the cardiovascular system with chapters on cardiac anatomy, physiology of myocardial contractility, cardiac output and oxygen delivery, and the autonomic nervous system. The next and subsequent years handbooks will be devoted to the basic sciences of respiratory, renal, endocrine, neurological and other systems. As with the previous editions, the course registrants presentations (or those that have been submitted on time) have also been included. The subjects that have been dealt with in the lectures and seminars (along with other reviews), that were included in previous handbooks are now published seperately in the journal Critical Care and Resuscitation. This handbook will still remain the working document of the Australasian Short Course on Intensive Care Medicine and is designed to supplement the course. During the sessions, you may find it useful to mark and note the text to facilitate your recall and review of the course at a later date. Along with the previous editions I trust that you find this edition useful. Dr. L.I.G. Worthley Adelaide, March 1999 vii viii Chapter 1 CARDIAC ANATOMY SURFACE ANATOMY In the adult cadaver about two-thirds of the heart is to the left of the midline. The outline of the heart may be drawn by connecting the points of the, lower border of the second left costal cartilage, 3.5 cm from the midline, to the upper border of the third right costal cartilage, 2.5 cm from the midline, to the sixth right costal cartilage, 2.5 cm from the midline, to the fifth left intercostal space, 9 cm from the midline. The relationship of the cardiac valves are shown in Fig 1.1. In a living erect person, the position of the heart may be 5 cm lower than in a cadaver.1 Fig. 1.1 Anteroposterior projection of the chest showing the outline of the heart and cardiac valves. CORONARY ARTERIES (Fig. 1.2) 1. The right coronary artery arises from the sinus of the right aortic cusp, passes forward between the root of the aortic trunk and the right auricle, then down between the right ventricle and the right atrium in the atrioventricular grove. At the junction of the right and inferior margin of the heart it gives off an acute marginal branch which travels along the inferior border of the right ventricle. The main artery then turns backward, passing between the atrioventricular grove of the inferior portion of the heart until it reaches the posterior interventricular grove, where it anastomoses with the left coronary artery. Near its termination it gives off a posterior interventricular branch and a posterolateral branch. The former runs forwards in the 1 Cardiac Anatomy interventricular grove, supplies branches to both ventricles and the posterior third of the intraventricular septum, and anastomoses near the apex of the heart with the left anterior descending branch of the left coronary artery. Fig. 1.2 Right and left coronary arteries and their branches. 2. The left coronary artery arises from the sinus of the left aortic cusp and passes forwards between the pulmonary trunk and the left auricle to divide into the left anterior descending and circumflex branches. The left anterior descending branch travels down towards the apex in the interventricular grove, giving off diagonal branches to supply the anterior surface of the left ventricle and septal branches to supply the anterior two-thirds of the intraventricular septum. The circumflex artery passes backwards in the atrioventricular grove, to supply the lateral and posterior portions of the left ventricle, with an obtuse marginal, and left lateral branches, anastomosing finally with the right coronary artery. In normal individuals, the right coronary artery is dominant (i.e., provides the major blood supply to the heart) in 50%, the left is dominant in 20%, and both left and right coronary arteries supply the heart equally in 30%. The posterior interventricular and the posterolateral branch usually arise from the circumflex artery when there is left coronary dominance.
Load more

Recommended publications
  • Cardiac Work and Contractility J
    Br Heart J: first published as 10.1136/hrt.30.4.443 on 1 July 1968. Downloaded from Brit. Heart 7., 1968, 30, 443. Cardiac Work and Contractility J. HAMER* It has been customary to regard the heart as a fibres is needed to maintain the stroke volume in a pump maintaining the flow of blood, and to assess larger ventricle, and ventricular work is correspon- the work done by the heart from the pressure and dingly reduced (Gorlin, 1962). Simple calcula- volume of blood leaving the ventricles. While cor- tions suggest that there is, in fact, little change in rect in physical terms, measurement of external work as the ventricle dilates (Table). The more cardiac work in this way is a poor index of the myo- forceful contraction produced by increased stretch- cardial oxygen consumption which is related to the ing of the muscle fibres through the Starling work done by the ventricular muscle. Systolic mechanism probably gives the dilated ventricle a pressure seems to be a more important determinant functional advantage. of ventricular work than stroke volume, and under Estimates of ventricular work based on force some conditions myocardial oxygen consumption measurements still give an incomplete picture of can be predicted from the systolic pressure, duration myocardial behaviour, as a rapid contraction needs of systole, and heart rate (Sarnoff et al., 1958). more energy than a slow one. The velocity of This relationship does not hold in other situations, contraction of the muscle fibres is an important as ventricular work depends on the force of the con- additional determinant of myocardial oxygen con- traction in the ventricular wall rather than on the sumption (Sonnenblick, 1966).
    [Show full text]
  • Optimal 131I Therapy of Thyrotoxicosis SNMMI Annual Meeting, 6/26/2018
    Optimal 131I Therapy of Thyrotoxicosis SNMMI Annual Meeting, 6/26/2018 I Love What I do, i.e. Nuclear Medicine … RADIOACTIVE IODINE THERAPY FOR No other relevant disclosures HYERTHYROIDISM Mark Tulchinsky, MD, FACNM, CCD or conflicts of interest Professor of Radiology and Medicine Division of Nuclear Medicine Penn State University Hospital Radioactive Iodine (RAI) Learning Objectives Administration for Graves’ • Treatment Options Disease: Birthplace of • Medications Radiotheranostics • Surgery Saul Hertz, M.D. • 131I Treatment (RAIT) (April 20, 1905 – July 28, 1950) • The first to study RAI in an • Graves’ Disease w/o Orbitopathy animal model of hyperthyroidism • Graves’ Disease with Orbitopathy • March 31st, 1941, at the age of 35 y, administered • Toxic Adenoma the first RAI treatment • Multinodular Toxic Goiter (RAIT) to a patient with Grave’s disease • Intermittent (recurrent) Thyroiditis • The first to use RAI uptake to inform RAIT, i.e. • Amiodarone Thyrotoxicosis radiotheranostic principle Therapeutic Options for Productive Conditions Amenable to RAIT Hyperthyroidism Condition Etiology • Antithyroid Drug therapy (ATDT) Graves’ disease (~80%) TSH-R-Ab stimulation of thyrocyte Symptomatic control with beta blockers Toxic Multinodular Goiter mutation → TSH-R-Ab activation → Toxic Adenoma autonomous function Thioureas, aka Thionamides, Anti- Hashimoto’s Thyroiditis in autoimmune disease - a variety of Thyroid Drugs (ATD’s) productive phase (“Hashi- cell- and antibody-mediated toxicosis”, overlaps Graves’) immune processes Corticosteroids
    [Show full text]
  • Time-Varying Elastance and Left Ventricular Aortic Coupling Keith R
    Walley Critical Care (2016) 20:270 DOI 10.1186/s13054-016-1439-6 REVIEW Open Access Left ventricular function: time-varying elastance and left ventricular aortic coupling Keith R. Walley Abstract heart must have special characteristics that allow it to respond appropriately and deliver necessary blood flow Many aspects of left ventricular function are explained and oxygen, even though flow is regulated from outside by considering ventricular pressure–volume characteristics. the heart. Contractility is best measured by the slope, Emax, of the To understand these special cardiac characteristics we end-systolic pressure–volume relationship. Ventricular start with ventricular function curves and show how systole is usefully characterized by a time-varying these curves are generated by underlying ventricular elastance (ΔP/ΔV). An extended area, the pressure– pressure–volume characteristics. Understanding ventricu- volume area, subtended by the ventricular pressure– lar function from a pressure–volume perspective leads to volume loop (useful mechanical work) and the ESPVR consideration of concepts such as time-varying ventricular (energy expended without mechanical work), is linearly elastance and the connection between the work of the related to myocardial oxygen consumption per beat. heart during a cardiac cycle and myocardial oxygen con- For energetically efficient systolic ejection ventricular sumption. Connection of the heart to the arterial circula- elastance should be, and is, matched to aortic elastance. tion is then considered. Diastole and the connection of Without matching, the fraction of energy expended the heart to the venous circulation is considered in an ab- without mechanical work increases and energy is lost breviated form as these relationships, which define how during ejection across the aortic valve.
    [Show full text]
  • Use of Analogy to Teach the Compensatory Mechanisms of the Heart in Heart Failure
    Saving Christmas: Use of Analogy to Teach The Compensatory Mechanisms of the Heart in Heart Failure. Krista L. Rompolski* *Corresponding Author: [email protected] HAPS Educator. Vol 22 (2), pp. 171-175. Published August 2018. doi: 10.21692/haps.2018.015 Rompolski K.L. (2018). Saving Christmas: Use of Analogy to Teach The Compensatory Mechanisms of the Heart in Heart Failure. HAPS Educator 22 (2): 171-175. doi: 10.21692/haps.2018.015 Saving Christmas: Use of Analogy to Teach The Compensatory Mechanisms of the Heart in Heart Failure Krista L. Rompolski, PhD, Drexel University, 1601 Cherry Street, Room 9115 Philadelphia, PA 19102 [email protected] Abstract Students of physiology are taught that the body’s homeostatic mechanisms are in place to maintain the body’s internal environment. This is most often associated with maintaining health. Congestive Heart Failure represents a disease in which the body’s homeostatic mechanisms worsen the progression of the disease. Using the analogy of Santa Claus delivering presents around the world in a single evening, students can gain a better understanding of how the body’s attempt to respond to a deviation from homeostasis, the decrease in cardiac output, may drive the progression of the disease. https://doi.org/10.21692/haps.2018.015 Key words: cardiac output, stroke volume, heart failure, RAAS Introduction Students of physiology and biology are taught the concept mechanisms include activation of the sympathetic nervous of homeostasis. The term was coined by Walter Cannon in system, ventricular hypertrophy with chronic remodeling, and 1932 in The Wisdom of the Body and used to describe the increased preload through activation of the renin-angiotensin- internal constancy of the body.
    [Show full text]
  • Cardiac Output
    Overview of Human Anatomy and Physiology: Cardiac Output Introduction Welcome to the Overview of Human Anatomy and Physiology course on the Cardiac System. This module, Cardiac Output, discusses measurement of heart activity and factors that affect activity. After completing this module, you should be able to: 1. Define stroke volume and cardiac output. 2. Discuss the relationship between heart rate, stroke volume, and cardiac output. 3. Identify the factors that control cardiac output. Measurement Cardiac Output The activity of the heart can be quantified to provide information on its health and efficiency. One important measurement is cardiac output (CO), which is the volume of blood ejected by the left ventricle each minute. Heart rate and stroke volume determine cardiac output. Heart rate (HR) is the number of heartbeats in one minute. The volume of blood ejected by the left ventricle during a heartbeat is the stroke volume (SV), which is measured in milliliters. Equation Cardiac output is calculated by multiplying the heart rate and the stroke volume. Average Values Cardiac output is the amount of blood pumped by the left ventricle--not the total amount pumped by both ventricles. However, the amount of blood within the left and right ventricles is almost equal, approximately 70 to 75 mL. Given this stroke volume and a normal heart rate of 70 beats per minute, cardiac output is 5.25 L/min. Relationships When heart rate or stroke volume increases, cardiac output is likely to increase also. Conversely, a decrease in heart rate or stroke volume can decrease cardiac output. What factors regulate increases and decreases in cardiac output? Regulation Factors Regulating Cardiac Output Factors affect cardiac output by changing heart rate and stroke volume.
    [Show full text]
  • The Radiochemistry of Bismuth
    NAS-NS-3061 RA OFBISMUTH NUCLEAR SCIENCE SERIES National Academy of Sciences - National Research Council Published by Technical Information Center ENERGY RESEARCH AND DEVELOPMENT ADMINISTRATION COMMITTEE ON NUCLEAR SCIENCE John Huizenga, Chairman, Nuclear WrUcture Re=arch Laboratory Thomas A. Tombrello, Vice Chairman, California institute of T=hnology C. K. Reed, Executive Secretary,Netional Academy of Sciences Lowell M. Bollinger, Argonne Nationel Laboratow Peggy Dyer, UnivarsiW of Washington Rusaall Heath, Aerojet Nuclear Co., Inc. Roy K. Middlaton, University of Pennsylvania 1: Lon Morgan, Columbie Scientific Industries G. Davis O’Kelley, Oek Ridge National Laboratow G. C. Phillips, Rice University Henry N. Wagner, Jr., The Johns Hopkins Medial Institutions Joseph Wen~, Brookhaven National Laboratory Sheldon’ Wolff, University of California Chien-Shiung Wu, Columbia Univar?@ Alexander Zuckar, Oak Ridga National Laborato~ Liaison Members William S. Rodney, National science Foundation George L. ROWS, Energy Research and Development Admini-ration SUBCOMMITTEE ON RAD1OCHEMISTRY G. Davis O’Kelley, Chairmsrr, Oak Ridge National Laboratory Glen E. Gordon, UnivwsiW of Maryler& ‘“- ,-. Rolfa H. Hw*r, Rutgers Univemity John A. Miskel, Lawrence Livermore LaboratoW Harold A. O’Brien, Jr., Los Alamos Scientific Laboratory Richard W. Perkins. Bettafle Pacific Northwest Laboratories Andrew F. Stehney, Argonne National Laboratory Kurt Wotfsbarg, Los Alanros Scientific Laboratow LiaisonMembers ~ John L. Burnatte, Energy Research and Davelopmant Administration FTed Findeis, National Scienca Foundation i.,.~.. Radiochemistry of Bismuth Kashinath S. Bhatki Tata Instituteof Fundamental Research Homi Bhabha Road, Bombay 400005 and Bhabha Atomic ResearchC-entre Trornbay,Bombay 400085 (India) Prepared for Subcommittee on Radiochemistry National Academy of Sciences - Natiorial Research Council IssuanceDate:September 1977 Published by Technical 1nform,ation center ENERGY RESEARCH AND DEVELOPMENT ADMINISTRATION Price$4.75.Availablefrom: NationalTechnicalInformationservice U.
    [Show full text]
  • Pesticides with Potential Thyroid Hormone-Disrupting Effects: a Review of Recent Data Michelle Leemans, Stephan Couderq, Barbara Demeneix, Jean-Baptiste Fini
    Pesticides With Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data Michelle Leemans, Stephan Couderq, Barbara Demeneix, Jean-Baptiste Fini To cite this version: Michelle Leemans, Stephan Couderq, Barbara Demeneix, Jean-Baptiste Fini. Pesticides With Po- tential Thyroid Hormone-Disrupting Effects: A Review of Recent Data. Frontiers in Endocrinology, Frontiers, 2019, 10, pp.743. 10.3389/fendo.2019.00743. hal-02415200 HAL Id: hal-02415200 https://hal.archives-ouvertes.fr/hal-02415200 Submitted on 26 Aug 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. REVIEW published: 09 December 2019 doi: 10.3389/fendo.2019.00743 Pesticides With Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data Michelle Leemans*, Stephan Couderq, Barbara Demeneix and Jean-Baptiste Fini* Muséum National d’Histoire Naturelle, CNRS UMR 7221, Laboratoire Physiologie moléculaire de l’adaptation, Paris, France Plant Protection Products, more commonly referred to as pesticides and biocides, are used to control a wide range of yield-reducing pests including insects, fungi, nematodes, and weeds. Concern has been raised that some pesticides may act as endocrine disrupting chemicals (EDCs) with the potential to interfere with the hormone systems of non-target invertebrates and vertebrates, including humans.
    [Show full text]
  • Synthesis and Nucleophilic Reactions of Bifunctional Thiourea S,S,S-Trioxides Dan Webb '89 Illinois Wesleyan University
    Illinois Wesleyan University Digital Commons @ IWU Honors Projects Chemistry 1989 Synthesis and Nucleophilic Reactions of Bifunctional Thiourea S,S,S-Trioxides Dan Webb '89 Illinois Wesleyan University Recommended Citation Webb '89, Dan, "Synthesis and Nucleophilic Reactions of Bifunctional Thiourea S,S,S-Trioxides" (1989). Honors Projects. Paper 30. http://digitalcommons.iwu.edu/chem_honproj/30 This Article is brought to you for free and open access by The Ames Library, the Andrew W. Mellon Center for Curricular and Faculty Development, the Office of the Provost and the Office of the President. It has been accepted for inclusion in Digital Commons @ IWU by the faculty at Illinois Wesleyan University. For more information, please contact [email protected]. ©Copyright is owned by the author of this document. • SynthesIs and Nucleophilic ReactIons of BIfunctional Thiourea S,S,S-TrIoxldes Dan Webb A ThesIs SubmItted In PartIal FulfIllment of the Requirements for Research Honors In ChemIstry at IllInois Wesleyan UnIversIty 1989 • ABSTRACT: The synthesis of bifunctional thioureas and the corresponding thiourea S,S,S-trioxides has been examined. Two methods for the synthesis of the bisthioureas were employed. One involved the treatment of a diamine with si1 icon tetraisothiocyanate in benzene. The second involved treatment of the amine with ammonium thiocyanate in dilute acid. This latter synthesis was superior because of the ease of its use, the high yields obtained, and the purity of the products. Though this synthesis worked well for the preparation of phenylene-l,4-bis(thiourea), it yielded only bisthiocyanate salts in the syntheses of al iphatic thioureas. The oxidation of the bisthioureas was carried out using peracetic acid or hydrogen peroxide to give the corresponding thiourea S,S,S-trioxides.
    [Show full text]
  • Comparative Pharmacotherapy of Thyroid
    ical C eut are ac & m H Mickael, J Pharma Care Health Sys 2015, S3 r e a a h l 10.4172/2376-0419.S3-002 t DOI: P h f S o y Journal of l s a t n e r m u s o J ISSN: 2376-0419 Pharmaceutical Care & Health Systems ReviewResearch Article Article OpenOpen Access Access Comparative Pharmacotherapy of Thyroid Diseases in Dogs and Cats--- What Should the Retail Pharmacist Filling Pet Prescriptions Understand? Marina Mickael, Eric Morris, Mollie M Roush and Inder Sehgal* Marshall University School of Pharmacy, West Virginia, USA Abstract Community pharmacies are increasingly receiving prescriptions from veterinarians for dogs and cats to receive human medications. However, retail pharmacists are not routinely trained in relevant aspects of veterinary-specific pharmacotherapy, such as, signs of improvement, time to improvement, drug administration techniques and potential adverse effects. Thyroid diseases in dogs and cats are treated with human-approved drugs that may be referred to pharmacies. Hypothyroidism is far more frequent in dogs, while hyperthyroidism is far more frequent in cats. Important comparative aspects of canine hypothyroidism pharmacotherapy can be summarized as follows: 1) Canine hypothyroid disease is similar to Hashimoto’s thyroiditis in humans in many of its signs and is treated using levothyroxine; 2) The doses of levothyroxine given to dogs are strikingly higher than in people; 3) A reasonable therapeutic goal is resolution of symptoms in two weeks to two months and a normal total T4 value (≈0.4-3.7 µg/dL). Important comparative
    [Show full text]
  • Drugs That Affect the Cardiovascular System
    PharmacologyPharmacologyPharmacology DrugsDrugs thatthat AffectAffect thethe CardiovascularCardiovascular SystemSystem TopicsTopicsTopics •• Electrophysiology Electrophysiology •• Vaughn-Williams Vaughn-Williams classificationclassification •• Antihypertensives Antihypertensives •• Hemostatic Hemostatic agentsagents CardiacCardiacCardiac FunctionFunctionFunction •• Dependent Dependent uponupon –– Adequate Adequate amountsamounts ofof ATPATP –– Adequate Adequate amountsamounts ofof CaCa++++ –– Coordinated Coordinated electricalelectrical stimulusstimulus AdequateAdequateAdequate AmountsAmountsAmounts ofofof ATPATPATP •• Needed Needed to:to: –– Maintain Maintain electrochemicalelectrochemical gradientsgradients –– Propagate Propagate actionaction potentialspotentials –– Power Power musclemuscle contractioncontraction AdequateAdequateAdequate AmountsAmountsAmounts ofofof CalciumCalciumCalcium •• Calcium Calcium isis ‘glue’‘glue’ that that linkslinks electricalelectrical andand mechanicalmechanical events.events. CoordinatedCoordinatedCoordinated ElectricalElectricalElectrical StimulationStimulationStimulation •• Heart Heart capablecapable ofof automaticityautomaticity •• Two Two typestypes ofof myocardialmyocardial tissuetissue –– Contractile Contractile –– Conductive Conductive •• Impulses Impulses traveltravel throughthrough ‘action‘action potentialpotential superhighway’.superhighway’. A.P.A.P.A.P. SuperHighwaySuperHighwaySuperHighway •• Sinoatrial Sinoatrial node node •• Atrioventricular Atrioventricular nodenode •• Bundle Bundle ofof
    [Show full text]
  • Cardiovascular Failure, Inotropes and Vasopressors
    Cardiovascular failure, inotropes and vasopressors Introduction thetensionintheventricularwallduring nantly affected by extrinsic factors sum- Cardiovascularfailure(‘shock’)meansthat diastoleastheheartfillswithbloodresult- marizedinTable 2. tissue perfusion is inadequate to meet inginstretchingofcardiacmusclefibres. metabolicdemandsforoxygenandnutri- Stretchingthefibresincreasestheforceof Oxygen delivery ents.Ifuncorrectedthiscanleadtoirre- contractionduringthesubsequentsystole Adequate oxygen delivery is dependent versible tissue hypoxia and cell death. (Frank–Starlingmechanismoftheheart). onboththecardiacoutputandthearte- Cardiovascularfailureisacommonindica- Afterloadisthetensionintheventricu- rial oxygen content. Most oxygen trans- tionforadmissiontothecriticalcareunit. lar wall required to eject blood into the portedinthebloodisboundtohaemo- Theaimoftreatmentistosupporttissue aorta. This will vary depending on the globin.Agramoffully-saturatedhaemo- perfusionandoxygendeliverywhichcan volume of the ventricle, the thickness of globin can carry 1.34ml of oxygen. beachievedthroughtheuseofvasoactive thewall,increasedsystemicvascularresist- Oxygen will also be dissolved in the drugs(inotropesandvasopressors). ance and the presence of conditions that plasma but the amount is negligible at Inotropes increase cardiac contractility obstructoutflow(e.g.aorticstenosis). normalatmosphericpressuresandthere- and cardiac output while vasopressors Contractility is the intrinsic ability of fore disregarded. Therefore the arterial cause vasoconstriction
    [Show full text]
  • Role of Myocardial Contractions on Coronary Vasoactivity
    MCB, vol.16, supplemental 2, pp.84-86, 2019 Role of Myocardial Contractions on Coronary Vasoactivity Xiao Lu1,* and Ghassan Kassab1 California Medical Innovations Institute, San Diego, CA 92121, USA. Corresponding Author: Xiao Lu. Email: [email protected]. Keywords: Extrinsic Pressure; coronary arterioles; mechanotransduction; heart failure; myocardial contractility; tachycardia Background: Heart failure (HF) is accompanied by alteration of hemodynamic conditions, which is due to the triggers of complex reflex changes in the sympathetic, endocrine, and rennin systems [1–2]. A critical effect of HF is reduced blood flow (ischemia) in the cardiovascular system resulting from mild to severe reduction in cardiac output (CO) due to dysfunction of myocardial contractility. It is known that coronary flow is regulated by many factors, including metabolic demand, perfusion pressure, oxidative stress, etc. Vascular vasodilation and vasoconstriction change microcirculation resistance and therefore regulate coronary circulation. However, it is not clear whether myocardial contractility may affect coronary tone to regulate coronary circulation in HF, i.e., the role the extrinsic mechanics in coronary arteriole tone. It is recognized that the extrinsic compression on blood vessel wall during skeletal muscle contraction is an independent regulator of vascular tone (3-4). Myocardial contraction also leads to such compression on intra-myocardial arterioles. Therefore, we hypothesize that myocardial contractility will change the arteriole tone to regulate
    [Show full text]